Nitric oxide (NO) and hydrogen sulfide (HS) are two gasotransmitters that are produced in the human body and have a key role in many of the physiological activities of the various organ systems. Decreased NO bioavailability and deficiency of HS are involved in the pathophysiology of type 2 diabetes and its complications. Restoration of NO levels have favorable metabolic effects in diabetes. The role of HS in pathophysiology of diabetes is however controversial; HS production is decreased during development of obesity, diabetes, and its complications, suggesting the potential therapeutic effects of HS. On the other hand, increased HS levels disturb the pancreatic β-cell function and decrease insulin secretion. In addition, there appear to be important interactions between NO and HS at the levels of both biosynthesis and signaling pathways, yet clear an insight into this relationship is lacking. HS potentiates the effects of NO in the cardiovascular system as well as NO release from its storage pools. Likewise, NO increases the activity and the expression of HS-generating enzymes. Inhibition of NO production leads to elimination/attenuation of the cardioprotective effects of HS. Regarding the increasing interest in the therapeutic applications of NO or HS-releasing molecules in a variety of diseases, particularly in the cardiovascular disorders, much is to be learned about their function in glucose/insulin metabolism, especially in diabetes. The aim of this review is to provide a better understanding of the individual and the interactive roles of NO and HS in carbohydrate metabolism.
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